A study from Darman et al predicted that mutant SF3B1‐induced cryptic 3′ splice site usage can introduce premature termination codons that are subjected to nonsense‐mediated decay (NMD) in approximately half of the aberrantly spliced transcripts.58 Some of the most well defined targets of this NMD such as ABCB7, SLC25A37, TMEM14C, and ALAS2 have provided some insights into a potential causal link between SF3B1 mutations and MDS‐RS. This evidence concerns the gene ABCB7 and myelodysplastic syndrome.